维生素D与心血管疾病：机制、流行病学证据与临床疗法的综合评估
Vitamin D and Cardiovascular Disease: A Comprehensive Evaluation of Mechanisms, Epidemiological Evidence, and Clinical Therapies
DOI: 10.12677/acm.2026.1672704, PDF,   
作者: 朱炟欣：首都医科大学肿瘤医学院，北京；王叙正*：首都医科大学第一临床医学院，北京
关键词: 维生素D；心血管疾病；分子机制；流行病学；阈值效应；临床干预；Vitamin D； Cardiovascular Disease； Molecular Mechanism； Epidemiology； Threshold Effect； Clinical Intervention
摘要: 心血管疾病(CVD)位居全球致死病因首位，疾病负担日趋严峻。维生素D除调控钙磷代谢外，可通过维生素D受体介导多通路参与心血管稳态调控。本文系统综述维生素D对CVD的保护机制、流行病学特征及临床研究进展。其心血管保护作用主要涉及：抑制NF-κB通路减轻血管炎症、提升内皮型一氧化氮合酶活性改善内皮功能、负向调控肾素–血管紧张素–醛固酮系统以稳定血压、优化糖脂代谢并促进胆固醇逆向转运延缓动脉粥样硬化、阻断Smad3通路抑制心肌纤维化与病理性重构。流行病学证据表明，血清25-羟维生素D (25(OH)D)与CVD风险呈显著阈值依赖性关联：25(OH)D < 50 nmol/L时CVD发病与死亡风险显著升高，50~74 nmol/L为风险过渡区间，≥75 nmol/L后保护效应趋于饱和，且该关联在老年、2型糖尿病、慢性肾病及肥胖等高危人群中更为突出。临床研究证实，常规补充维生素D无法降低普通人群的主要不良心血管事件风险，仅对维生素D缺乏及特定高危亚群获益明确，每日≤ 4000 IU剂量安全性良好。目前国内外指南不推荐大剂量维生素D用于CVD常规一级预防，仅建议针对性纠正维生素D缺乏。现有研究结论存在异质性与争议，主要受基线维生素D水平、干预方案及混杂因素影响。未来需针对重度维生素D缺乏、代谢异常等高危人群开展大样本、长期随机对照研究，结合多组学技术完善机制与个体化干预证据，推动维生素D在CVD精准防治中的规范化应用。
Abstract: Cardiovascular disease (CVD) remains the leading cause of global death with a growing disease burden. Beyond its classical role in calcium and phosphorus homeostasis, vitamin D exerts extensive regulatory effects on cardiovascular pathophysiology via vitamin D receptor-dependent signaling pathways. This review systematically summarizes the protective mechanisms, epidemiological characteristics, and clinical evidence of vitamin D in CVD. Vitamin D protects the cardiovascular system by inhibiting NF-κB-mediated inflammation, improving endothelial function by upregulating endothelial nitric oxide synthase activity, stabilizing blood pressure through negative regulation of the renin-angiotensin-aldosterone system, delaying atherosclerosis via optimizing glycolipid metabolism and reverse cholesterol transport, and suppressing Smad3-dependent myocardial fibrosis and pathological remodeling. Epidemiological studies demonstrate a clear threshold effect of serum 25-hydroxyvitamin D (25(OH)D) on CVD risk. Low 25(OH)D level (<50 nmol/L) significantly increases CVD incidence and mortality; 50~74 nmol/L represents a risk transition range; and the protective effect plateaus at ≥75 nmol/L without further benefits, especially in high-risk populations including the elderly, type 2 diabetes, chronic kidney disease, and obese patients. Clinical evidence indicates that routine vitamin D supplementation fails to reduce major adverse cardiovascular events in the general population, whereas targeted supplementation benefits vitamin D-deficient and high-risk subgroups with good safety at a daily dose ≤ 4000 IU. Current guidelines do not support high-dose vitamin D for routine CVD primary prevention and only recommend correcting established vitamin D deficiency. Heterogeneous study results are mainly attributed to baseline vitamin D status, variable intervention regimens, and confounding factors. Future large-scale, long-term randomized controlled trials focusing on precisely defined high-risk populations, together with multi-omics mechanistic exploration, are required to optimize individualized intervention strategies and standardize the precise application of vitamin D in CVD prevention and treatment.
文章引用：朱炟欣, 王叙正. 维生素D与心血管疾病：机制、流行病学证据与临床疗法的综合评估[J]. 临床医学进展, 2026, 16(7): 1803-1817. https://doi.org/10.12677/acm.2026.1672704

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